Table 2. Clinical observations of the use of HVPG in predicting liver-related outcomes associated with NAFLD.
| Author (year) | Study type (origin) | Study subjects | Major findings | Notes |
|---|---|---|---|---|
| Sourianarayanane et al (2017)52 | Retrospective (USA) | 142 patients with biopsy-proven chronic liver disease (including 35 patients with NASH and 52 patients with chronic HCV infection) undergoing HVPG assessment | HVPG was on average 4 mmHg lower in patients with NASH as compared to those with HCV for each stage of fibrosis | 5 of 19 patients (26.3%) with NASH and 10 of 31 (32.4%) patients with chronic HCV infection had HVPG>6 mmHg in the presence of ≤F2 fibrosis |
| Sanyal et al (2019)54 | Retrospective (80 centers in North America and Europe) | 475 patients with NASH and F3 to F4 fibrosis previously enrolled in two clinical trials evaluating simtuzumab in NAFLD | Among the 50 patients who developed a major liver-related clinical event (e.g., ascites, encephalopathy, variceal bleed) over an average of 5 months of follow-up, HVPG was <10 mmHg in seven (14%) | HVPG-based prediction of decompensation in NAFLD is less reliable than seen in the landmark trial of 213 patients with cirrhosis of diverse etiologies by Ripoll et al.9 |
| Ferrusquia-Acosta et al (2021)53 | Cross-sectional (Spain, Italy) | 120 patients with cirrhosis due to NASH (n=40), alcohol (n=40), and chronic HCV infection (n=40) undergoing HVPG measurement and TIPS placement | Discrepancy between indirect (via HVPG) and direct (via TIPS) measurement of portal pressure was independently associated with NASH etiology of cirrhosis | Lower HVPG threshold may be required to predict decompensation events in NAFLD-associated cirrhosis |
| Pons et al (2021)56 | Retrospective (Spain, France, Romania, Italy, Austria, Canada, Switzerland, UK) | 836 patients with compensated advanced chronic liver disease of various etiologies (including 248 patients with NAFLD) undergoing simultaneous HVPG and LSM | LSM predicted significantly lower prevalence of portal hypertension (HVPG>5 mmHg) in NAFLD (61%) vs. other etiologies (>90%) | Discrepancies in the use of LSM cutoffs to predict HVPG-based portal hypertension in NAFLD demonstrate need for additional studies to validate both methods in this setting |
| Bassegoda et al (2022)55 | Cross-sectional (20 centers in Europe) | 548 patients with advanced NAFLD and 444 patients with advanced chronic HCV infection undergoing HVPG measurement | 15 of 166 patients (9%) with advanced NAFLD and HVPG 5.5 to 9 mmHg had evidence of decompensation | Patients with advanced NAFLD may experience decompensation even with subclinical portal hypertension, indicating the need for different HVPG cutoffs |
HCV, hepatitis C virus; HVPG, hepatic venous pressure gradient; LSM, liver stiffness measurement; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; TIPS, transjugular intrahepatic portosystemic shunt.